Abstract
Overexpression of the c-myc proto-oncogene features prominently in most human cancers. Early studies established that inhibiting the expression of oncogenic c-myc, produced potent anti-cancer effects. This gave rise to the notion that an appropriate c-myc silencing agent might provide a broadly applicable and more effective form of cancer treatment than is currently available. The endogenous mechanism of RNA interference (RNAi), through which small RNA molecules induce gene silencing by binding to complementary mRNA transcripts, represents an attractive avenue for c-myc inhibition. However, the development of a clinically viable, anti-c-myc RNAi-based platform is largely dependent upon the design of an appropriate carrier of the effector nucleic acids. To date, organic and inorganic nanoparticles were assessed both in vitro and in vivo, as carriers of small interfering RNA (siRNA), DICER-substrate siRNA (DsiRNA), and short hairpin RNA (shRNA) expression plasmids, directed against the c-myc oncogene. We review here the various anti-c-myc RNAi-based nanosystems that have come to the fore, especially between 2005 and 2020.
Highlights
The c-myc gene encodes a nuclear phosphoprotein that is widely recognized for its role as a transcription factor
We review here the various anti-c-myc RNA interference (RNAi)-based nanosystems that have come to the fore, especially between 2005 and 2020
The oncogenic activity of c-myc can be eliminated by inhibiting the expression of the activated gene, inhibiting inter-protein associations that are critical for c-Myc function, or by overhangs that typify small interfering RNA (siRNA), termed DICER-substrate siRNA (DsiRNA), can induce RNAi, with a reportedly higher efficiency
Summary
The c-myc gene encodes a nuclear phosphoprotein that is widely recognized for its role as a transcription factor. Short dsRNA molecules, lacking the dinucleotide tolerated over time [32] These findings, together with an estimation that c-myc is deregulated in up to 70% of human cancers [18], making it the most frequently altered oncogene, motivate strongly for the therapeutic value of inhibiting oncogenic c-myc. The oncogenic activity of c-myc can be eliminated by inhibiting the expression of the activated gene, inhibiting inter-protein associations that are critical for c-Myc function, or by overhangs that typify siRNA, termed DICER-substrate siRNA (DsiRNA), can induce RNAi, with a reportedly higher efficiency. DNA-directed RNAi, a strategy that generates specific siRNA molecules in vivo, is a useful gene-silencing tool [41] This involves the construction of a RNA pol-driven plasmid expression vector, into which an antigene sequence of at least 19 nucleotides is inserted, together with appropriate termination signals. This review discusses the potential application of anti-c-myc RNAi nanosystems in cancer treatment
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